To the Editor: We describe a patient with malignant ascites and bacterial peritonitis, with no apparent intra-abdominal source of infection.

A 56-year-old woman with advanced breast cancer was admitted to hospital with a 10-day history of diffuse abdominal pain, umbilical tenderness, and increasing abdominal girth. Breast cancer had been diagnosed 13 years before admission (T2 N0 M0) and treated with radical mastectomy and adjuvant chemotherapy. Five years before admission, disease had recurred at the chest wall, and 2 years before, liver metastases were found. Chemotherapy had failed, and her only current treatment comprised capecitabine and analgesics.

On admission, the patient had tachycardia (110 beats per min), tachypnoea (26 breaths per min), blood pressure of 115/80 mmHg, and no fever or signs of sepsis. Examination showed evidence of local recurrence around the left mastectomy scar, and marked ascites with discoloration, warmth, tenderness and a diffuse infiltration over the umbilicus. There were no signs of peritoneal irritation, nor leg oedema.

Blood test results were in the normal range, except for mild leukocytosis (10.6 × 109 cells/L; reference range [RR], 3.8–9.8 × 109 cells/L), with left shift (86% neutrophils, and 6% lymphocytes; RR, up to 67% neutrophils, and at least 32% lymphocytes). X-ray did not show abdominal free air. Abdominal computed tomography revealed ascites, retroperitoneal lymph nodes, omental and umbilical infiltration, and the known liver metastases without signs of portal hypertension.

Peritoneal tap removed 2800 mL of fluid. Examination of the fluid revealed a white blood cell count of 2 × 109 cells/L (80% neutrophils), glucose concentration of 790 g/L, and albumin concentration of 22 g/L (serum–ascites albumin gradient, 0.7; a gradient < 1.1 indicates that the patient does not have portal hypertension).

Gram stain of the ascitic fluid revealed gram-positive cocci, and culture identified Staphylococcus aureus. Cytological examination showed sheets of atypical enlarged epithelial cells highly suggestive of malignancy. Therapy was begun with parenteral cloxacillin and ciprofloxacin, but the patient died shortly after.

This patient’s condition is unlikely to have been spontaneous (“primary”) bacterial peritonitis, which usually occurs in patients with liver cirrhosis, portal hypertension and ascites with high serum–ascites albumin gradient,1 and occasionally in patients with malignant ascites.2 However, in our patient, infection may have originated from the umbilical metastasis. The umbilicus has a direct connection with the intra-abdominal cavity and is also connected to a number of intra-abdominal organs via embryological remnants, such as the umbilical vein and the urachus. Both routes may be involved in the spread of malignant tumour to the umbilicus,3 but spread may also be in the opposite direction, causing peritonitis.

This diagnosis may be missed by physicians who may not notice anything new in a patient with longstanding malignant ascites, and may fail to consider bacterial peritonitis, a treatable condition.